Serum interleukin-17 (IL-17) fell by approximately 72% with curcumin and more than doubled with placebo over 2 months in male patients with COPD, according to a triple-blind randomized trial presented at CHEST 2026 in Phoenix.¹

Among 68 patients randomized to curcumin (n = 34) or placebo (n = 34), IL-17 in the curcumin group fell from 71.85 ± 61.81 pg/mL at baseline to 42.34 ± 27.52 pg/mL at 2 weeks and 20.08 ± 20.08 pg/mL at 2 months (P <.001).¹ Levels in the placebo group held steady at 2 weeks (45.81 ± 33.23 pg/mL; P =.531) before climbing to 101.71 ± 39.64 pg/mL at 2 months (P <.001 vs baseline), when the between-group difference reached significance (P <.001).¹

IL-17A drives neutrophilic airway inflammation in COPD, and preclinical data link it to inflammatory cell recruitment and show its expression rises in response to pathogens common in COPD airways.² Curcumin, a turmeric-derived polyphenol, regulates several inflammatory mediators, although evidence in pulmonary disease comes largely from in vitro and animal models. Curcumin's poor oral bioavailability has complicated its use in humans.³

The authors positioned curcumin as a potential adjunct to bronchodilators and inhaled corticosteroids for suppressing neutrophilic inflammation, and they called for larger multicenter trials using standardized formulations and clinical outcome measures.¹ In the following Q&A, investigator Retno Ariza Soemarwoto, MD, from Lampung University in Indonesia, discusses the rise in IL-17 among patients receiving placebo, the team’s formulation choice, and what a guideline-ready trial would require.

Q&A: Curcumin Lowers IL-17 in COPD, With Retno Ariza Soemarwoto, MD

HCPLive: What is the main takeaway from this trial that you’d want pulmonologists and primary care clinicians managing COPD to know?

Soemarwoto: The main takeaway is that curcumin may help reduce inflammation and improve respiratory symptoms in patients with COPD. Improvements were observed after 2 weeks and persisted through 60 days, as reflected by reduced cough and breathlessness scores.

HCPLive: What led your team to focus on IL-17 specifically, and how does it fit into the neutrophilic inflammation picture in COPD that current inhaled therapies don’t fully address?

Soemarwoto: IL-17, mainly IL-17A from Th17 cells, drives the neutrophilic inflammation that is typical of COPD. It induces airway epithelial cells to release neutrophil chemokines such as CXCL1 and CXCL8, increases mucus production, and contributes to airway remodeling and alveolar destruction. Curcumin has preclinical and early clinical evidence of suppressing Th17 differentiation.

HCPLive: What curcumin formulation and dose did you use, and how did you address curcumin’s bioavailability challenges?

Soemarwoto: We chose 1 g/day, and we gave it for 60 days. We used a turmeric oil and turmeric aqueous extract formulation to overcome curcumin’s poor bioavailability. This technology has been reported to provide approximately 10-fold higher bioavailability than standard 95% curcuminoids and around 6-fold and 5-fold higher total curcuminoid absorption than essential-oil and phospholipid formulations.

HCPLive: The curcumin group had greater baseline IL-17 levels. How should clinicians interpret the 72% reduction in light of this difference?

Soemarwoto: The higher baseline IL-17 levels in the curcumin group may be partly explained by the greater burden of comorbidities and the higher frequency of exacerbations in that group, both of which could contribute to increased systemic inflammation.

[A] 72% reduction in IL-17 should be interpreted cautiously, ideally by comparing changes from baseline between the curcumin and placebo groups and adjusting for relevant baseline factors.

HCPLive: IL-17 more than doubled in the placebo group by 2 months. What explains that rise?

Soemarwoto: The rise in IL-17 levels in the placebo group may be partly explained by the higher frequency of exacerbations during the study, as reflected by worsening cough and breathlessness. These clinical changes may indicate increased airway inflammation. In addition, the study period coincided with the rainy season, which may have contributed to respiratory infections and COPD exacerbations.

HCPLive: The trial enrolled only male patients. What was the reasoning behind that, and how confident are you that these findings would extend to women with COPD?

Soemarwoto: We included only male patients to reduce potential confounding factors associated with sex differences, particularly hormonal influences and other biological variations that may affect inflammatory responses.

HCPLive: How should clinicians respond when patients with COPD ask about over-the-counter turmeric or curcumin supplements?

Soemarwoto: Our study showed promising improvements in COPD symptoms as early as 14 days using a curcumin formulation containing turmeric oil and turmeric aqueous extract. This formulation was designed to improve curcumin bioavailability.

HCPLive: What would the next trial need to look like for curcumin to earn a place in COPD guidelines?

Soemarwoto: The next step would be a larger, multicenter clinical trial involving both male and female patients to improve the generalizability of the findings. The study should have a longer follow-up period and focus on clinically meaningful outcomes, particularly COPD exacerbation rates, quality of life, and symptom control, in addition to inflammatory biomarkers such as IL-17. It would also be important to evaluate the safety and consistency of the specific curcumin formulation used.

References

1. Ariza R, Meirissa T, Hendarto G, et al. Curcumin as an adjunct therapy suppresses serum interleukin-17 in chronic obstructive pulmonary disease patients: a randomized controlled trial. Presented at: CHEST 2026; October 20, 2026; Phoenix, AZ.

2. Ritzmann F, Beisswenger C. Preclinical studies and the function of IL-17 cytokines in COPD. Ann Anat. 2021;237:151729. doi:10.1016/j.aanat.2021.151729

3. Lelli D, Sahebkar A, Johnston TP, Pedone C. Curcumin use in pulmonary diseases: state of the art and future perspectives. Pharmacol Res. 2017;115:133-148. doi:10.1016/j.phrs.2016.11.017